2016
Pro-recombination Role of Srs2 Protein Requires SUMO (Small ubiquitin-like Modifier) but Is Independent of PCNA (Proliferating Cell Nuclear Antigen) Interaction
KOLESÁR, Peter; Veronika ALTMANNOVÁ; Sonia SILVA; Michael LISBY; Lumír KREJČÍ et. al.Základní údaje
Originální název
Pro-recombination Role of Srs2 Protein Requires SUMO (Small ubiquitin-like Modifier) but Is Independent of PCNA (Proliferating Cell Nuclear Antigen) Interaction
Autoři
KOLESÁR, Peter; Veronika ALTMANNOVÁ; Sonia SILVA; Michael LISBY a Lumír KREJČÍ
Vydání
Journal of Biological Chemistry, Bethesda, American Society for Biochemistry and Molecular Biology Inc. 2016, 0021-9258
Další údaje
Jazyk
angličtina
Typ výsledku
Článek v odborném periodiku
Obor
Genetika a molekulární biologie
Stát vydavatele
Spojené státy
Utajení
není předmětem státního či obchodního tajemství
Impakt faktor
Impact factor: 4.125
Kód RIV
RIV/00216224:14110/16:00088201
Organizační jednotka
Lékařská fakulta
UT WoS
000383447600032
EID Scopus
2-s2.0-84964844250
Klíčová slova anglicky
DNA repair; Homologous recombination; Possible mechanisms; Post-translational modifications; Proliferating cell nuclear antigens; Recombination factors; Small ubiquitin-like modifiers; Sumoylation
Příznaky
Mezinárodní význam, Recenzováno
Změněno: 28. 11. 2016 16:09, Ing. Mgr. Věra Pospíšilíková
Anotace
V originále
Srs2 plays many roles in DNA repair, the proper regulation and coordination of which is essential. Post-translational modification by small ubiquitin-like modifier (SUMO) is one such possible mechanism. Here, we investigate the role of SUMO in Srs2 regulation and show that the SUMO-interacting motif (SIM) of Srs2 is important for the interaction with several recombination factors. Lack of SIM, but not proliferating cell nuclear antigen (PCNA)-interacting motif (PIM), leads to increased cell death under circumstances requiring homologous recombination for DNA repair. Simultaneous mutation of SIM in a srs2 deltaPIM strain leads to a decrease in recombination, indicating a pro-recombination role of SUMO. Thus SIM has an ambivalent function in Srs2 regulation; it not only mediates interaction with SUMO-PCNA to promote the anti-recombination function but it also plays a PCNA-independent pro-recombination role, probably by stimulating the formation of recombination complexes. The fact that deletion of PIM suppresses the phenotypes of Srs2 lacking SIM suggests that proper balance between the anti-recombination PCNA-bound and pro-recombination pools of Srs2 is crucial. Notably, sumoylation of Srs2 itself specifically stimulates recombination at the rDNA locus.
Návaznosti
| EE2.3.30.0009, projekt VaV |
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| EE2.3.30.0037, projekt VaV |
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| GAP207/12/2323, projekt VaV |
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| GA13-26629S, projekt VaV |
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| MUNI/M/1894/2014, interní kód MU |
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| ROZV/20/LF/2015, interní kód MU |
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